Reprogramming of CTLs into natural killer-like cells in celiac disease

Autor: Veronique M. Braud, Gerasim A. Orbelyan, Cezary Ciszewski, Bana Jabri, Daniel E. Geraghty, Peter H.R. Green, Govind Bhagat, Carol E. Semrad, Emily O. Kistner, Robert Winchester, Stefano Guandalini, Maria Tretiakova, Bertrand Meresse, Mala Setty, Leanne Lee, Lewis L. Lanier, Shane A. Curran
Přispěvatelé: University of Chicago, Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS), Columbia University [New York], COMUE Université Côte d'Azur (2015-2019) (COMUE UCA), University of California SF (UNIVERSITY OF CALIFORNIA), University of California, Fred Hutchinson Cancer Research Center [Seattle] (FHCRC)
Jazyk: angličtina
Rok vydání: 2006
Předmět:
MESH: Signal Transduction
MESH: Intestine
Small
Lymphoma
MESH: Base Sequence
0302 clinical medicine
Intestinal mucosa
Interferon
Intestine
Small
Immunology and Allergy
Cytotoxic T cell
Interferon gamma
Intestinal Mucosa
Phosphorylation
Receptors
Immunologic
Receptor
0303 health sciences
ZAP-70 Protein-Tyrosine Kinase
Cell Differentiation
hemic and immune systems
Articles
MESH: Gene Expression Regulation
3. Good health
Killer Cells
Natural
Cytomegalovirus Infections
MESH: Intestinal Mucosa
Signal transduction
medicine.drug
Signal Transduction
MESH: Killer Cells
Natural
MESH: Cell Differentiation
MESH: Interferon Type II
Immunology
Molecular Sequence Data
chemical and pharmacologic phenomena
Biology
Article
03 medical and health sciences
Interferon-gamma
MESH: Gene Expression Profiling
MESH: Cell Proliferation
medicine
Humans
[SDV.BBM]Life Sciences [q-bio]/Biochemistry
Molecular Biology
MESH: Receptors
Immunologic
030304 developmental biology
Cell Proliferation
MESH: Molecular Sequence Data
MESH: Humans
Base Sequence
MESH: Phosphorylation
Gene Expression Profiling
MESH: Chronic Disease
MESH: ZAP-70 Protein-Tyrosine Kinase
MESH: Cytomegalovirus Infections
CTL
Celiac Disease
Gene Expression Regulation
MESH: Protein Processing
Post-Translational
Chronic Disease
Cytokine secretion
MESH: Lymphoma
Protein Processing
Post-Translational
MESH: T-Lymphocytes
Cytotoxic
MESH: Celiac Disease
030215 immunology
T-Lymphocytes
Cytotoxic
Zdroj: Journal of Experimental Medicine
Journal of Experimental Medicine, Rockefeller University Press, 2006, 203 (5), pp.1343-55. ⟨10.1084/jem.20060028⟩
The Journal of Experimental Medicine
Meresse, Bertrand; Curran, Shane A; Ciszewski, Cezary; Orbelyan, Gerasim; Setty, Mala; Bhagat, Govind; et al.(2006). Reprogramming of CTLs into natural killer-like cells in celiac disease. Journal of Experimental Medicine, 203(5), 1343-1355. UC San Francisco: Retrieved from: http://www.escholarship.org/uc/item/75x6r369
ISSN: 0022-1007
1540-9538
DOI: 10.1084/jem.20060028⟩
Popis: Celiac disease is an intestinal inflammatory disorder induced by dietary gluten in genetically susceptible individuals. The mechanisms underlying the massive expansion of interferon γ–producing intraepithelial cytotoxic T lymphocytes (CTLs) and the destruction of the epithelial cells lining the small intestine of celiac patients have remained elusive. We report massive oligoclonal expansions of intraepithelial CTLs that exhibit a profound genetic reprogramming of natural killer (NK) functions. These CTLs aberrantly expressed cytolytic NK lineage receptors, such as NKG2C, NKp44, and NKp46, which associate with adaptor molecules bearing immunoreceptor tyrosine-based activation motifs and induce ZAP-70 phosphorylation, cytokine secretion, and proliferation independently of T cell receptor signaling. This NK transformation of CTLs may underlie both the self-perpetuating, gluten-independent tissue damage and the uncontrolled CTL expansion leading to malignant lymphomas in severe forms of celiac disease. Because similar changes were detected in a subset of CTLs from cytomegalovirus-seropositive patients, we suggest that a stepwise transformation of CTLs into NK-like cells may underlie immunopathology in various chronic infectious and inflammatory diseases.
Databáze: OpenAIRE
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